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To explore the role of insulin-like growth factor 1 (IGF-1) gene expression abnormality in neurotrophic causes of diabetic peripheral neurophathy.Methods. Diabetes was induced in Sprague Dawley rats by alloxan. The parameters were measured as follows: IGF-1 mRNA by reverse transcriptase-polymerase chain reaction (RT-PCR); IGF-1 peptide by enzyme-linked immunosorbent assay (ELISA); electrophysiological parameters of nerves by evoked electromyo-gram; morphometric evaluation of sciatic nerves under light microscope and transmission electron microscope.Results. During early diabetic stage, IGF-1 mRNA [ (0. 430 ±0. 031) vs. (0. 370 ±0. 016), P <0. 01, (0. 430 ±0. 031) vs. (0. 280 ±0. 010) , P <0. 001, respectively], IGF - 1 peptide contents [ (38. 44 ±3. 60) ng/mg vs. (30. 06 ±2. 41) ng/mg, P <0. 01, (38. 44 ± 3. 6) ng/mg vs. (3. 71 ±2. 70) ng/mg, P <0. 001, respectively] in sciatic nerve tissue reduced in diabetic rats with hyperglycemia and varied with severity of diabetic state when compared with n
To explore the role of insulin-like growth factor 1 (IGF-1) gene expression abnormality in neurotrophic causes of diabetic peripheral neurophathy. Methods. Diabetes was induced in Sprague Dawley rats by alloxan. The parameters were measured as follows: IGF- 1 mRNA by reverse transcriptase-polymerase chain reaction (RT-PCR); IGF-1 peptide by enzyme-linked immunosorbent assay (ELISA); electrophysiological parameters of nerves by evoked electromyo- gram; morphometric evaluation of sciatic nerves under light microscope and transmission electron microscope. Results During early diabetic stage, IGF-1 mRNA (0. 430 ± 0. 031 vs. 0. 370 ± 0. 016, P <0.01, (0. 430 ± 0. 031) vs. (0. 280 ± 0. 010), P <0. 001, respectively], IGF - 1 peptide contents [(38.44 ± 3.60) ng / mg vs. (30.06 ± 2.41) ng / mg, P <0.01, (38.44 ± 3.6) ng / mg vs. (3.71 ± 2.70) ng / mg, P <0.001, respectively] in sciatic nerve tissue reduced in diabetic rats with hyperglycemia and varied with severity of diabetic state w hen compared with n